IRAK4 as a molecular target in the amelioration of innate immunity-related endotoxic shock and acute liver injury by chlorogenic acid

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dc.contributor.authorS H Park-
dc.contributor.authorS I Baek-
dc.contributor.authorJi Eun Yun-
dc.contributor.authorS Lee-
dc.contributor.authorD Y Yoon-
dc.contributor.authorJ K Jung-
dc.contributor.authorS H Jung-
dc.contributor.authorB Y Hwang-
dc.contributor.authorJ T Hong-
dc.contributor.authorS B Han-
dc.contributor.authorY Kim-
dc.date.accessioned2017-04-19T10:01:04Z-
dc.date.available2017-04-19T10:01:04Z-
dc.date.issued2015-
dc.identifier.issn0022-1767-
dc.identifier.uri10.4049/jimmunol.1402101ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/12415-
dc.description.abstractMice lacking the IL-1R-associated kinase 4 (IRAK4) are completely resistant to LPS-induced endotoxic disorder or the TLR9 agonist CpG DNA plus D-galactosamine-induced acute liver injury (ALI), whereas wild-type strains succumb. However, translational drugs against sepsis or ALI remain elusive. Lonicerae flos extract is undergoing the clinical trial phase I in LPS-injected healthy human volunteers for sepsis treatment. In the current study, chlorogenic acid (CGA), a major anti-inflammatory constituent of lonicerae flos extract, rescued endotoxic mortality of LPS-intoxicated C57BL/6 mice, as well as ameliorated ALI of LPS/D-galactosamine-challenged C57BL/6 mice. As a mechanism, CGA inhibited various TLR agonist-, IL-1α-, or high-mobility group box-1-stimulated autophosphorylation (activation) of IRAK4 in peritoneal macrophages from C57BL/6 or C3H/HeJ mice via directly affecting the kinase activity of IRAK4, a proximal signal transducer in the MyD88-mediated innate immunity that enhances transcriptional activity of NF-κB or AP-1. CGA consequently attenuated protein or mRNA levels of NF-κB/AP-1 target genes encoding TNF-α, IL-1α, IL-6, and high-mobility group box-1 in vivo under endotoxemia or ALI. Finally, this study suggests IRAK4 as a molecular target of CGA in the treatment of innate immunity-related shock and organ dysfunction following insult of various TLR pathogens from bacteria and viruses.-
dc.publisherAmer Assoc Immunologists-
dc.titleIRAK4 as a molecular target in the amelioration of innate immunity-related endotoxic shock and acute liver injury by chlorogenic acid-
dc.title.alternativeIRAK4 as a molecular target in the amelioration of innate immunity-related endotoxic shock and acute liver injury by chlorogenic acid-
dc.typeArticle-
dc.citation.titleJournal of Immunology-
dc.citation.number3-
dc.citation.endPage1130-
dc.citation.startPage1122-
dc.citation.volume194-
dc.contributor.affiliatedAuthorJi Eun Yun-
dc.contributor.alternativeName박선홍-
dc.contributor.alternativeName백승일-
dc.contributor.alternativeName윤지은-
dc.contributor.alternativeName이승민-
dc.contributor.alternativeName윤다영-
dc.contributor.alternativeName정재경-
dc.contributor.alternativeName정상훈-
dc.contributor.alternativeName황방연-
dc.contributor.alternativeName홍진태-
dc.contributor.alternativeName한상배-
dc.contributor.alternativeName김영수-
dc.identifier.bibliographicCitationJournal of Immunology, vol. 194, no. 3, pp. 1122-1130-
dc.identifier.doi10.4049/jimmunol.1402101-
dc.description.journalClassY-
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